Pathophysiology - Cracking Plaques
- Foundation: Atherosclerosis leads to vulnerable plaques in coronary arteries.
- Plaque Morphology: Characterized by a thin, rupture-prone fibrous cap over a large, inflammatory lipid-rich necrotic core.
- The Event: Spontaneous or stress-induced rupture/erosion of the plaque exposes its highly thrombogenic contents (e.g., collagen, tissue factor) to the blood.
- Thrombus Formation: This triggers rapid platelet adhesion and aggregation, forming a non-occlusive, platelet-rich (white) thrombus.
- Result: The thrombus reduces coronary blood flow, causing myocardial ischemia and anginal symptoms, but without complete vessel blockage.
⭐ Unstable Angina (UA) and NSTEMI exist on a continuum, sharing the same pathophysiology. The key difference is the severity and duration of ischemia: in UA, it's insufficient to cause detectable myocyte necrosis (i.e., cardiac biomarkers are negative).
Clinical Presentation & Diagnosis - The Heart's Cry
- Chest Pain: Retrosternal, crushing/pressure, radiating to arm/jaw.
- New onset: Severe, limiting activity.
- Crescendo: ↑ frequency, duration, or intensity.
- At rest: Lasting > 20 minutes.
- Physical Exam: Often normal; may show diaphoresis, S4 gallop, or signs of heart failure.

⭐ Key Discriminator: Unstable Angina is defined by the absence of elevated cardiac enzymes (troponins). It represents myocardial ischemia without infarction.
Risk Stratification - Scoring Severity
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TIMI Score: Estimates mortality for patients with UA/NSTEMI. One point for each risk factor.
-
HEART Score: Predicts 6-week risk of Major Adverse Cardiac Events (MACE).
⭐ HEART Score Components: History, ECG, Age, Risk factors, Troponin. A score of 0-3 is low risk and supports discharge.

Management - Code Red Care
Initial therapy aims to stabilize the patient and prevent further thrombosis.
📌 MONA-BASH
- Morphine: For refractory angina.
- Oxygen: Supplemental, only if O₂ saturation < 90%.
- Nitrates: Sublingual or IV for active pain. ⚠️ Caution: Avoid in hypotension, RV infarction, or recent PDE5 inhibitor use.
- Antiplatelet Therapy:
- Aspirin (162-325 mg) chewed immediately, followed by daily 81 mg.
- P2Y12 inhibitor (e.g., clopidogrel, ticagrelor).
- Beta-blocker: Start within 24 hours if no signs of heart failure or shock.
- Anticoagulation: LMWH (enoxaparin) or UFH.
- Statin: High-intensity (e.g., Atorvastatin 80 mg) initiated early.
⭐ In cocaine-induced ACS, avoid beta-blockers due to the risk of unopposed alpha-stimulation. Use benzodiazepines for anxiety and sympathetic surge.
High‑Yield Points - ⚡ Biggest Takeaways
- Unstable Angina is new-onset, accelerating, or rest angina representing acute myocardial ischemia.
- It is distinguished from NSTEMI by normal cardiac biomarkers; there is no myocardial necrosis.
- EKG findings are often transient ST-segment depression or T-wave inversions, but can be normal.
- Caused by a non-occlusive thrombus over a disrupted atherosclerotic plaque.
- Management focuses on antiplatelet and anticoagulant therapy to prevent progression to MI.
- Risk stratification (e.g., TIMI score) is crucial to guide timing for angiography.
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